دورية أكاديمية

Actin-binding proteins differentially regulate endothelial cell stiffness, ICAM-1 function and neutrophil transmigration.

التفاصيل البيبلوغرافية
العنوان: Actin-binding proteins differentially regulate endothelial cell stiffness, ICAM-1 function and neutrophil transmigration.
المؤلفون: Schaefer A; Department of Molecular Cell Biology, Sanquin Research and Landsteiner Laboratory, Academic Medical Center and Swammerdam Institute of Life Sciences, University of Amsterdam, 1066 CX Amsterdam, The Netherlands a.schaefer@sanquin.nl p.hordijk@sanquin.nl., Te Riet J; Department of Tumor Immunology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, Nijmegen 6525 GA, The Netherlands., Ritz K; Department of Pathology, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands., Hoogenboezem M; Department of Molecular Cell Biology, Sanquin Research and Landsteiner Laboratory, Academic Medical Center and Swammerdam Institute of Life Sciences, University of Amsterdam, 1066 CX Amsterdam, The Netherlands., Anthony EC; Department of Molecular Cell Biology, Sanquin Research and Landsteiner Laboratory, Academic Medical Center and Swammerdam Institute of Life Sciences, University of Amsterdam, 1066 CX Amsterdam, The Netherlands., Mul FP; Department of Molecular Cell Biology, Sanquin Research and Landsteiner Laboratory, Academic Medical Center and Swammerdam Institute of Life Sciences, University of Amsterdam, 1066 CX Amsterdam, The Netherlands., de Vries CJ; Department of Medical Biochemistry, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands., Daemen MJ; Department of Pathology, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands., Figdor CG; Department of Tumor Immunology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, Nijmegen 6525 GA, The Netherlands., van Buul JD; Department of Molecular Cell Biology, Sanquin Research and Landsteiner Laboratory, Academic Medical Center and Swammerdam Institute of Life Sciences, University of Amsterdam, 1066 CX Amsterdam, The Netherlands., Hordijk PL; Department of Molecular Cell Biology, Sanquin Research and Landsteiner Laboratory, Academic Medical Center and Swammerdam Institute of Life Sciences, University of Amsterdam, 1066 CX Amsterdam, The Netherlands a.schaefer@sanquin.nl p.hordijk@sanquin.nl.
المصدر: Journal of cell science [J Cell Sci] 2014 Oct 15; Vol. 127 (Pt 20), pp. 4470-82. Date of Electronic Publication: 2014 Aug 08.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Company of Biologists Country of Publication: England NLM ID: 0052457 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1477-9137 (Electronic) Linking ISSN: 00219533 NLM ISO Abbreviation: J Cell Sci Subsets: MEDLINE
أسماء مطبوعة: Publication: Cambridge : Company of Biologists
Original Publication: London.
مواضيع طبية MeSH: Transendothelial and Transepithelial Migration*, Actinin/*metabolism , Endothelial Cells/*metabolism , Filamins/*metabolism , Intercellular Adhesion Molecule-1/*metabolism , Marine Toxins/*metabolism , Neutrophils/*physiology , Plaque, Atherosclerotic/*metabolism, Actinin/genetics ; Actins/metabolism ; Animals ; Cell Adhesion/genetics ; Endothelial Cells/cytology ; Filamins/genetics ; HeLa Cells ; Humans ; Male ; Marine Toxins/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Plaque, Atherosclerotic/genetics
مستخلص: Chronic vascular inflammation is driven by interactions between activated leukocytes and the endothelium. Leukocyte β2-integrins bind to endothelial intercellular adhesion molecule 1 (ICAM-1), which allows leukocyte spreading, crawling and transendothelial migration. Leukocytes scan the vascular endothelium for permissive sites to transmigrate, which suggests that there is apical membrane heterogeneity within the endothelium. However, the molecular basis for this heterogeneity is unknown. Leukocyte adhesion induces ICAM-1 clustering, which promotes its association to the actin-binding proteins filamin B, α-actinin-4 and cortactin. We show that these endothelial proteins differentially control adhesion, spreading and transmigration of neutrophils. Loss of filamin B, α-actinin-4 and cortactin revealed adaptor-specific effects on a nuclear-to-peripheral gradient of endothelial cell stiffness. By contrast, increasing endothelial cell stiffness stimulates ICAM-1 function. We identify endothelial α-actinin-4 as a key regulator of endothelial cell stiffness and of ICAM-1-mediated neutrophil transmigration. Finally, we found that the endothelial lining of human and murine atherosclerotic plaques shows elevated levels of α-actinin-4. These results identify endothelial cell stiffness as an important regulator of endothelial surface heterogeneity and of ICAM-1 function, which in turn controls the adhesion and transmigration of neutrophils.
(© 2014. Published by The Company of Biologists Ltd.)
التعليقات: Erratum in: J Cell Sci. 2014 Nov 15;127(22):4985.
Erratum in: J Cell Sci. 2014 Oct 15;127(Pt 20):doi/10.1242/jcs.164814.
فهرسة مساهمة: Keywords: Adhesion; Endothelium; Inflammation; Transmigration
المشرفين على المادة: 0 (ACTN4 protein, human)
0 (Actins)
0 (Filamins)
0 (Marine Toxins)
11003-00-2 (Actinin)
126547-89-5 (Intercellular Adhesion Molecule-1)
132579-38-5 (contractin A)
تواريخ الأحداث: Date Created: 20140810 Date Completed: 20151113 Latest Revision: 20141015
رمز التحديث: 20221213
DOI: 10.1242/jcs.154708
PMID: 25107367
قاعدة البيانات: MEDLINE
الوصف
تدمد:1477-9137
DOI:10.1242/jcs.154708